Essentially, the heart is a pump which pumps blood throughout the body. It consists of four chambers, including a left atrium, a right atrium, a left ventricle and a right ventricle. In order for the heart to efficiently perform its function as a pump, the atrial muscles and ventricular muscles should contract in a proper sequence and in a timed relationship.
In a given cardiac cycle (corresponding to one “beat” of the heart), the two atria contract, forcing the blood therein into the ventricles. A short time later, the two ventricles contract, forcing the blood therein to the lungs (from the right ventricle) or through the body (from the left ventricle). Meanwhile, blood from the body fills the right atrium and blood from the lungs fills the left atrium, waiting for the next cycle to begin. A typical healthy adult heart may beat at a rate of 60–70 beats per minute (bpm) while at rest, and may increase its rate to 140–180 bpm when the adult is engaging in strenuous physical exercise, or undergoing other physiologic stress.
The healthy heart controls its rhythm from its sinoatrial (SA) node, located in the upper portion of the right atrium. The SA node generates an electrical impulse at a rate commonly referred to as the “sinus” rate. This impulse is delivered to the atrial tissue when the atria are to contract and, after a suitable delay, propagates to the ventricular tissue when the ventricles are to contract.
When the atria contract, a detectable electrical signal referred to as a P-wave is generated. When the ventricles contract, a detectable electrical signal referred to as the QRS complex (also referred to simply an “R-wave”) is generated, as a result of the depolarization of the ventricles. The R-wave is much larger than the P-wave, principally because the ventricular muscle tissue is much more massive than the atrial muscle tissue. The atrial muscle tissue need only produce a contraction sufficient to move the blood a very short distance—from the respective atrium to its corresponding ventricle. The ventricular muscle tissue, on the other hand, must produce a contraction sufficient to push the blood over a long distance (e.g., through the complete circulatory system of the entire body).
It is the function of a pacemaker to provide electrical stimulation pulses to the appropriate chamber(s) of the heart (atria and/or ventricles) in the event the heart is unable to beat on its own (e.g., in the event either the SA node fails to generate its own natural stimulation pulses at an appropriate sinus rate, or in the event such natural stimulation pulses do not effectively propagate to the appropriate cardiac tissue). Most modern pacemakers accomplish this function by operating in a “demand” mode where stimulation pulses from the pacemaker are provided to the heart only when it is not beating on its own, as sensed by monitoring the appropriate chamber of the heart for the occurrence of a P-wave or an R-wave. If a P-wave or an R-wave is not sensed within a prescribed period of time (which period of time is often referred to as the “escape interval”), then a stimulation pulse is generated at the conclusion of this prescribed period of time and delivered to the appropriate heart chamber via a pacemaker lead.
Modern programmable pacemakers are generally of two types: (1) single chamber pacemakers, and (2) dual-chamber pacemakers. In a single chamber pacemaker, the pacemaker provides stimulation pulses to, and senses cardiac activity within, a single-chamber of the heart (e.g., either the right ventricle or the right atrium). In a dual-chamber pacemaker, the pacemaker provides stimulation pulses to, and senses cardiac activity within, two chambers of the heart (e.g., both the right atrium and the right ventricle). The left atrium and left ventricle can also be paced, provided that suitable electrical contacts are made therewith.
During atrial tracking bi-ventricular pacing, pacing or sensing occurs in the atria, then (after a programmed time period) pacing occurs in the ventricles. In this manner, the bi-ventricular pacing tracks the rate of the atria (where the heart beat starts). Unfortunately, in some instances, a given patient may develop fast atrial rhythms which result from a pathologic arrhythmia such as a pathologic tachycardia, fibrillation or flutter. In these cases, non-mode-switching dual-chamber pacemakers can pace the ventricles in response to the sensed atrial arrhythmia only up to the programmed maximum tracking rate (MTR). This, however, will allow the ventricles to intrinsically beat in a deleterious non-synchronous manner when the intrinsic rate is greater than the MTR.
Standard modern dual-chamber pacemakers now prevent undesirable tracking of certain atrial arrhythmias by automatically switching the pacemaker's mode of operation from an atrial tracking pacing mode to a non-atrial tracking pacing mode. For example, U.S. Pat. No. 4,722,341 to Hedberg et al., teaches an atrium-controlled pacemaker, where the pacemaker temporarily switches from an atrial tracking mode to a non-atrial tracking mode for a fixed number of stimulation pulses if the sensed atrial activity indicates an atrial arrhythmia may be developing. This behavior has carried over to bi-ventricular devices, even though it may be less appropriate under those circumstances
During atrial fibrillation (AF), a standard modern dual-chamber bradycardia pacemaker switches to a non-atrial tracking mode to prevent rapid, irregular ventricular pacing. However, when the intrinsic ventricular response to the AF is faster than the pacing rate, pacing is inhibited. While this is an appropriate response for a standard demand type bradycardia pacemaker, which is designed to prevent the patient's heart rate from falling below a certain minimum limit, it is not appropriate for newer devices targeted to patients with heart failure (HF). For HF patients, whose pacemakers pace both ventricles (referred to as bi-ventricular pacing or BiV pacing), the benefit of the device is best realized with continuous, or nearly continuous, bi-ventricular pacing. Thus, during rapidly conducted AF, a different response is needed to maximize bi-ventricular pacing.
More specifically, when a patient goes into AF, the typical response of a BiV pacemaker (also referred to herein simply as “the device”) is to switch from an atrial tracking mode to a non-atrial tracking mode to prevent the fast, irregular tracking of the atrial fibrillation by the device. When the device mode switches, it typically goes to either a fixed BiV pacing rate, or to an adjustable BiV pacing rate that provides rate response based on the patient's level of activity or other available indicators of the patient's physiologic need. For the sake of consistency, the BiV pacing rate during mode switch (i.e., during a non-atrial tracking bi-ventricular pacing mode) will be hereafter referred to as the “mode switch base rate” or simply as “MSBR”. If the patient's intrinsic rate is above the MSBR, the pacemaker's output is inhibited. For HF patients with devices that deliver BiV pacing, such inhibition of pacing negates the benefit of cardiac resynchronization that BiV pacing is intended to confer. Specifically, if the patient remains in AF for long periods of time, this can have a deleterious effect on the patient's clinical condition. It would be advantageous if such deleterious effects can be reduced and preferably minimized.